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Related Concept Videos

Telomeres and Telomerase02:41

Telomeres and Telomerase

In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.
Telomeres and Telomerase02:41

Telomeres and Telomerase

In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.
Homologous Recombination02:31

Homologous Recombination

The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
Homologous Recombination02:31

Homologous Recombination

The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...

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Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
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Published on: April 13, 2015

Telomeric recombination induced by dysfunctional telomeres.

Marie Eve Brault1, Chantal Autexier

  • 1Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec, Canada H3A 2B2.

Molecular Biology of the Cell
|December 2, 2010
PubMed
Summary

Telomere dysfunction can trigger recombination-based telomere maintenance in cancer cells. This finding is crucial for understanding alternative cancer cell survival mechanisms beyond telomerase.

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Area of Science:

  • Oncology
  • Cell Biology
  • Genetics

Background:

  • Telomere maintenance is critical for cancer cell immortality.
  • Most cancers rely on telomerase for telomere maintenance, a key anticancer target.
  • A subset of cancers uses alternative recombination-based mechanisms for telomere maintenance.

Purpose of the Study:

  • To investigate if telomere dysfunction can promote recombination-based telomere maintenance.
  • To explore alternative pathways for cancer cell survival when telomerase is inhibited.

Main Methods:

  • Induction of telomere dysfunction in human cancer cells.
  • Analysis of telomeric recombination events.
  • Comparison of telomere maintenance mechanisms in cancer cell lines.

Main Results:

  • Telomeric recombination was successfully induced in human telomerase-positive cancer cells.
  • Dysfunctional telomeres were shown to promote recombination-based telomere maintenance.
  • This represents a novel mechanism of telomere maintenance in cancer.

Conclusions:

  • Telomere dysfunction is a potent inducer of recombination-based telomere maintenance.
  • This pathway offers a potential mechanism for cancer cells to evade telomerase-targeted therapies.
  • Understanding this process is vital for developing novel anticancer strategies.